Multiple models have been generated to describe the underlying neural circuitry that gives rise to the GBO. Two prominent ones include the Interneuron Network Gamma (ING) model and the Pyramidal Interneuron Network Gamma (PING) model (102). In the ING, pyramidal cells are synchronized by the activity of interneurons, but pyramidal cells themselves are not directly involved in the generation of the GBO. In PING, oscillations are generated via the recurrent synaptic connectivity between the excitatory activity of pyramidal cells and feedback inhibition of interneurons. While this process is still not fully understood, experimental observations favor the PING model of GBO generation. In this case, synaptic inhibition via GABAergic interneurons defines the timing and firing rate of pyramidal neurons, creating precise windows within which large groups of excitatory cells can fire synchronously (103–105). In turn, excitatory cells also provide input onto GABAergic interneurons, creating a loop for entrainment of cortical networks across brain regions. Support for the PING model comes from findings that interneuron activity follows pyramidal cell activity by a short delay, consistent with pyramidal cell excitatory drive as the main stimulus for interneuron excitation in the model (106, 107). Within excitatory cells, α1-containing GABAA receptors post-synaptic to a subset of inhibitory interneuron processes produce currents with decay periods fitting for the production of gamma oscillations (84). Lastly, it has been shown that with genetic knockout of AMPA glutamate receptors within specific populations of inhibitory interneurons, synaptic excitation of these inhibitory interneurons is diminished and the power of the gamma oscillation severely reduced (108). These findings support the theory that the GBO arises from a complicated interplay between excitatory pyramidal cells and inhibitory interneurons.